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PubMed1977

Effects of sodium nitroprusside on left ventricular diastolic pressure-volume relations.

The effect of sodium nitroprusside on the relationship between left ventricular pressure and volume during diastole was studied in 11 patients with congestive heart failure. Nitroprusside was infused to lower mean arterial pressure approximately 20-30 mm Hg. High fidelity left ventricular pressures were recorded in all patients simultaneously with left ventricular cineangiography (biplane in eight and single plane in three patients), allowing precise measurement of pressure and volume throughout the cardiac cycle. Left ventricular diastolic pressure-volume curves were constructed in each patient from data obtained before and during nitroprusside infusion. In 9 of 11 patients there was a substantial downward displacement of the diastolic pressure-volume curve during nitroprusside infusion, with left ventricular pressure being lower for any given volume with nitroprusside. Serial left ventricular cineangiograms performed 15 min apart in six additional subjects who did not receive sodium nitroprusside showed no shift in the diastolic pressure-volume relation, indicating that the shift seen with nitroprusside was not due to the angiographic procedure itself. A possible explanation for the altered diastolic pressure-volume relationships with nitroprusside might be a direct relaxant effect of nitroprusside on ventricular muscle, similar to its known relaxant effect on vascular smooth muscle. Alternatively, nitroprusside may affect the diastolic pressure-volume curve by affecting viscous properties or by altering one or more of the extrinsic constraints acting upon the left ventricle.

Aorta↗
PubMed1987

A clinical study of sensitivity to sodium nitroprusside during controlled hypotensive anesthesia in young and elderly patients.

Aging has important effects on the cardiovascular system; baroreceptor reflex function decreases and the elderly are more resistant to both beta-receptor agonists and antagonists. The purpose of the present clinical study was to determine the relationship between age and sensitivity to sodium nitroprusside in 16 patients during deliberate hypotensive anesthesia by determining the blood pressure changes in young and elderly patients to incremental increases in dose of sodium nitroprusside. A dose-response curve relating change in mean blood pressure to dose of sodium nitroprusside (microgram X kg-1 X min-1) was constructed for each patient; the slope of this line is a measure of "sensitivity." The change in mean arterial blood pressure per microgram X kg-1 X min-1 nitroprusside dose (i.e., slope), showed a significant correlation with age (r = 0.766, P less than 0.001), demonstrating that sensitivity to sodium nitroprusside increases with advancing years. The maximum change in heart rate produced by nitroprusside showed a reciprocal correlation with age (r = -0.791, P less than 0.001). There was no significant correlation between age and maximum change in plasma norepinephrine or epinephrine concentrations during nitroprusside infusion. The increased sensitivity to nitroprusside might have been due to diminished baroreflex activity, resistance of cardiac adrenergic receptors to catecholamine stimulation, or alteration in sensitivity to the direct vasodilating effects of sodium nitroprusside. Whatever the mechanism, however, this clinical study has shown that lower doses of nitroprusside should be used in elderly patients to achieve the same degree of hypotension achieved in younger patients.

Adolescent↗
PubMed1996

Localized administration of sodium nitroprusside enhances its protection against platelet aggregation in stenosed and injured coronary arteries.

Sodium nitroprusside, a potent vasodilator, was evaluated for its effect on platelet aggregation in stenosed and endothelium-injured coronary arteries in a canine model. Twenty-five anesthetized dogs were studied; coronary blood flow velocity was continuously monitored. Recurrent intracoronary platelet aggregation and dislodgment (indicated by cyclic variations in coronary blood flow) were induced by mechanically injuring and stenosing the left anterior descending coronary artery. Sodium nitroprusside was administered either intrapericardially or intravenously 30 min after cyclic flow variations were established. Intrapericardial administration of saline (control) did not affect cyclic flow variations in any of 6 tested dogs. Sodium nitroprusside abolished cyclic flow variations in all 7 dogs (100%) when given intrapericardially and in 5 to 7 dogs (71%) when given intravenously (compared to intrapericardial salines, p < 0.01). A smaller dose of sodium nitroprusside was required to abolish cyclic flow variations when given intrapericardially than when given intravenously (1.6 +/- 0.5 micrograms.kg-1.min-1 vs 4.8 +/- 0.8 micrograms.kg-1.min-1, p < 0.01). The mean aortic pressure was reduced by 10 to 20 mmHg after intrapericardial sodium nitroprusside administration and by 30 to 40 mmHg after intravenous sodium nitroprusside administration. To investigate the mechanism of protection by sodium nitroprusside, NG-monomethyl-L-arginine, an inhibitor of nitric oxide synthetase, was used to induce cyclic flow variations in mildly injured and stenosed left anterior descending coronary arteries in 5 dogs. Intrapericardial sodium nitroprusside abolished the cyclic flow variations in all 5 dogs. Then oxyhemoglobin, an inhibitor of nitric oxide, was administered into the left anterior descending coronary arteries of these dogs, and it restored the sodium nitroprusside-abolished cyclic flow variations in all 5 dogs. Thus, sodium nitroprusside protects against platelet aggregation and cyclic flow variations in stenosed and endothelium-injured canine coronary arteries, probably by the action of nitric oxide, and it is more effective and hemodynamically safer when administered intrapericardially than when administered intravenously.

Administration, Topical↗
PubMed1982

Effects of nitroprusside on pancreatic juice secretion in the blood-perfused canine pancreas.

The effects of nitroprusside on the secretion of pancreatic juice were investigated in preparations of isolated and blood-perfused canine pancreas. Nitroprusside (10-30 micrograms/kg) injected intravenously elicited a dose-dependent increase in pancreatic secretion accompanied by a decrease in blood pressure. Intra-arterial administration of nitroprusside (3-300 micrograms) into the perfused pancreas also elicited an increased secretion in preparations of both constant pressure and constant flow perfusion system. The results suggest that nitroprusside-induced pancreatic secretion may not result from the peripheral vasodilatation caused by nitroprusside. The effect of 100 micrograms of intra-arterial nitroprusside corresponded roughly to that of 0.1 units of secretin or 0.3 units of pancreozymin. Nitroprusside-induced secretion was inhibited by the infusion of ethacrynic acid (1 mg/min), but was not modified by phentolamine, propranolol, atropine, haloperidol, tetrodotoxin and metiamide. Nitroprusside produced a dose-dependent increase in the bicarbonate and protein concentrations in the juice, but had little effect on chloride concentration. This action was different from that of secretin or pancreozymin. It is concluded that nitroprusside may produce an increase in pancreatic secretion by acting directly on pancreatic cells, and that this action may be mediated at least in part through the increase of intracellular cyclic GMP concentration.

Animals↗
PubMed1982

The hemodynamic response to dopamine and nitroprusside following right atrium-pulmonary artery bypass (Fontan procedure).

Cardiac output is critically dependent upon pulmonary vascular resistance after right atrium-pulmonary artery bypass (Fontan procedure), since there is no pulmonary ventricle in the circulation. Inotropic agents, including dopamine, may increase pulmonary vascular resistance and, therefore, might have an adverse effect on cardiac output. The present study determined the hemodynamic responses to dopamine and nitroprusside of 9 patients following right atrium-pulmonary artery bypass. Particular attention was given to effects on cardiac output (CI), pulmonary vascular resistance, and right atrial pressure (RAP). Baseline hemodynamic data were measured without drugs, with dopamine at 7.5 micrograms/kg/min, with sodium nitroprusside up to 5.0 micrograms/kg/min, and with a combination of dopamine, 7.5 micrograms/kg/min, and sodium nitroprusside, 1.0 micrograms/kg/min. Right and left atrial pressures (LAP), mean arterial blood pressure (BP), heart rate (HR), and CI were measured. Stroke volume index and pulmonary arteriolar resistance index were calculated. The increase in CI from baseline (1.98 +/- 0.86 liters per minute) was significant for infusions of dopamine (2.75 +/- 1.05, p less than 0.001), sodium nitroprusside (2.57 +/- 0.78, p less than 0.001), and both drugs (2.74 +/- 0.84, p less than 0.001). The increased CI was achieved primarily by a significant increase in HR with dopamine and by an increase in stroke volume index with sodium nitroprusside. With a similar increment in CI, the RAP was significantly decreased from baseline (21 +/- 4 torr) with sodium nitroprusside (15 +/- 3, p less than 0.001) but was unchanged with dopamine. Pulmonary arteriolar resistance index decreased significantly from baseline (375 +/- 230 dynes sec cm-5/m2) with sodium nitroprusside (169 +/- 132, p less than 0.001), and, interestingly, with dopamine as well (273 +/- 165, p less than 0.05). Both dopamine and sodium nitroprusside in these dosages have favorable effects on CI and pulmonary arteriolar resistance index in patients after right atrium-pulmonary artery bypass. Whenever feasible, sodium nitroprusside is preferred for increasing CI after such a bypass procedure, since lower RAP decreases the severity of fluid retention, ascites, and chest tube drainage.

Adolescent↗
PubMed2000

S-nitroso-N-acetylpenicillamine and nitroprusside induce apoptosis in a neuronal cell line by the production of different reactive molecules.

CHP212 neuroblastoma cells were exposed to two different nitric oxide (NO) donors, S-nitroso-N-acetylpenicillamine and sodium nitroprusside. Apoptosis and necrosis were determined with flow cytometric analysis of annexin V binding and propodium iodide uptake. Both S-nitroso-N-acetylpenicillamine and sodium nitroprusside induced apoptosis, but with a different time dependency. Oxyhemoglobin (NO scavenger) attenuated the toxicity of S-nitroso-N-acetylpenicillamine, but had no effect on the toxicity of sodium nitroprusside. By contrast, deferoxamine (iron chelator) attenuated the toxicity of sodium nitroprusside, but had no effect on the toxicity of S-nitroso-N-acetylpenicillamine. Urate (ONOO(-) scavenger) did not influence the toxicity of either S-nitroso-N-acetylpenicillamine or sodium nitroprusside, but protected from SIN-1 (3-morpholinosydnonimine, ONOO(-) donor). It was shown that both dithiothreitol and ascorbic acid affected the toxicity of S-nitroso-N-acetylpenicillamine and sodium nitroprusside in opposite ways. In the presence of dithiothreitol, superoxide dismutase and catalase decreased the toxicity of sodium nitroprusside. In the presence of cells, but not in their absence, S-nitroso-N-acetylpenicillamine decomposed with a half-life of about 4 h as assessed by the production of nitrite and absorbance reduction at 335 nm. Sodium nitroprusside decomposed very slowly in the presence of cells as assessed by the production of ferrocyanide. It can be concluded that (1) slow and sustained release of NO from S-nitroso-N-acetylpenicillamine at the cell surface causes apoptosis in CHP212 cells, probably without the involvement of ONOO(-), (2) sodium nitroprusside causes apoptosis by the production of H(2)O(2) and/or iron, rather than NO, and probably has to be taken up by the cell for decomposition.

1-Methyl-4-phenylpyridinium↗
PubMed1998

Apparent role of hydroxyl radicals in oxidative brain injury induced by sodium nitroprusside.

Sodium nitroprusside (disodium nitroferricyanide) has been suggested to cause cytotoxicity through either the release of cyanide and/or nitric oxide. The present study investigated a possible mechanism that after a brief release of nitric oxide, iron moiety of breakdown products of sodium nitroprusside could cause a long lasting oxidative stress, such as hydroxyl radical generation, lipid peroxidation and cytotoxicity. Intranigral administration of sodium nitroprusside (0-16.8 nmol) to rats induced an acute increase in lipid peroxidation in the substantia nigra and a chronic dopamine depletion in the caudate nucleus. Photodegraded (nitric oxide-exhausted) sodium nitroprusside, however, still produced lipid peroxidation and neurotoxicity in the midbrain. Moreover, non-iron containing nitric oxide-donor compounds, such as S-nitroso-N-acetylpenicillamine, did not cause oxidative brain injury in vivo suggesting that nitric oxide may not mediate neurotoxicity induced by sodium nitroprusside. Additional in vitro studies demonstrated that both freshly prepared (nitric oxide donor) and photodegraded (nitric oxide-exhausted) sodium nitroprusside generated hydroxyl radicals in the presence of ascorbate and also increased lipid peroxidation in brain homogenates. These pro-oxidative effects of sodium nitroprusside were blocked by nitric oxide, S-nitroso-N-acetylpenicillamine, oxyhemoglobin, and deferoxamine (iron chelator). The present results suggest that iron moiety, rather than nitric oxide, may mediate the pro-oxidative properties of sodium nitroprusside. With this new information in mind, the misuse of sodium nitroprusside as a selective nitric oxide donor in both basic and clinical uses should be urgently addressed.

Animals↗
PubMed1982

Hemodynamic effects of nitroprusside and furosemide in left ventricular failure.

Nitroprusside and furosemide are both used to treat acute left ventricular failure, but their hemodynamic effects have not been compared in the same patients. In 13 patients with acutely decompensated chronic left ventricular failure, we infused nitroprusside to reduce pulmonary wedge pressure to normal without inducing hypotension. When hemodynamics returned to control after stopping nitroprusside, furosemide was given ase a 200-mg rapid infusion. Control hemodynamic values before each drug were in the same range. Mean arterial pressure fell from 99.9 +/- 16.7(SD) to 74.8 +/- 10.5 mm Hg on nitroprusside (P less than 0.001) and was unchanged after furosemide. Nitroprusside reduced pulmonary wedge pressure from 30.5 +/- 6.9 to 15.9 to 6.0 mm Hg (P less than 0.001), while furosemide reduced it to 27.5 +/- 8.5 mm Hg (P less than 0.05). Cardiac index rose from 2.33 +/- 0.78 l/min/m2 to 3.62 +/- 0.93 l/min/m2 (P less than 0.001) on nitroprusside and remained unchanged at 2.32 +/- 0.64 l/min/m2 after furosemide. At the same pulmonary wedge pressure on each drug (24 mg Hg), cardiac index was increased by nitroprusside (+0.6 +/- 0.5 l/min/m2, P less than 0.01) and unchanged by furosemide. Thus, furosemide reduces only preload without changing cardiac output in patients with left heart failure, whereas nitroprusside at similar or lower preload in the same patients reduces afterload and raises cardiac output and improves left ventricular performance. Nitroprusside appears preferable for the immediate treatment of left ventricular failure.

Aged↗
PubMed1984

Photodegradation of sodium nitroprusside: biologic activity and cyanide release.

Because the belief that cyanide is released from nitroprusside in vivo recently was challenged, the authors performed a series of experiments that examined the conditions under which nitroprusside is degraded. These experiments include an examination of the release of cyanide and nitric oxide from nitroprusside in vitro, the release of cyanide in vivo, and a comparison of the biologic activity of intact and degraded nitroprusside. Nitroprusside in aqueous solution degraded when exposed to white or blue light but not to red light. While light at 20 microW X cm-2 produced 40% apparent photodegradation after 6 h exposure, while white light at 220 microW X cm-2 produced 100% apparent photodegradation after 2 h exposure. At 10% apparent photodegradation, 10% of the nitrosyl ligand was recovered as free nitric oxide, and 0.4% of the cyanide ligand was recovered as free cyanide. Following a 2-h infusion of light-protected nitroprusside in seven patients, cyanide concentrations ranged from 1.4 to 45.5 microM and 0.09 to 3.2 microM in blood and plasma, respectively. These values were not changed by exposing the samples to white light (220 microW X cm-2) for 4 h. Intact and photodegraded nitroprusside produced identical hypotensive responses in rats as would be expected, since the nitrosyl ligand was detected in solution following degradation, and it mediates this action. Cyanide was released from nitroprusside, both on its exposure to light in vitro and also in vivo. The latter was not an artifact of the assay for cyanide. Nitroprusside releases cyanide in vivo, and cyanide toxicity is a true complication of its use.

Animals↗
PubMed2002

Intracarotid nitroprusside does not augment cerebral blood flow in human subjects.

BACKGROUND: The recent resurgence of interest in the cerebrovascular effects of nitroprusside can be attributed to the possibility of using nitric oxide donors in treating cerebrovascular insufficiency. However, limited human data suggest that intracarotid nitroprusside does not directly affect cerebrovascular resistance. In previous studies, physiologic or pharmacologic reactivity of the preparation was not tested at the time of nitroprusside challenge. The authors hypothesized that if nitric oxide is a potent modulator of human cerebral blood flow (CBF), then intracarotid infusion of nitroprusside will augment CBF. METHODS: Cerebral blood flow was measured (intraarterial (133)Xe technique) in sedated human subjects undergoing cerebral angiography during sequential infusions of (1) intracarotid saline, (2) intravenous phenylephrine to induce systemic hypertension, (3) intravenous phenylephrine with intracarotid nitroprusside (0.5 microg x kg(-1) x min(-1)), and (4) intracarotid verapamil (0.013 mg x kg(-1) x min(-1)). Data (mean +/- SD) were analyzed by repeated-measures analysis of variance and post hoc Bonferroni-Dunn test. RESULTS: Intravenous phenylephrine increased systemic mean arterial pressure (from 83 +/- 12 to 98 +/- 6 mmHg; n = 8; P < 0.001), and concurrent infusion of intravenous phenylephrine and intracarotid nitroprusside reversed this effect. However, compared with baseline, CBF did not change with intravenous phenylephrine or with concurrent infusions of intravenous phenylephrine and intracarotid nitroprusside. Intracarotid verapamil increased CBF (43 +/- 9 to 65 +/- 11 ml x 100 g(-1) x min(-1); P < 0.05). CONCLUSIONS: The authors conclude that, in humans, intracarotid nitroprusside sufficient to decrease mean arterial pressure during recirculation, does not augment CBF. Failure of intracarotid nitroprusside to augment CBF despite demonstrable autoregulatory vasoconstriction and pharmacologic vasodilation questions the significance of nitric oxide-mediated vasodilation in human cerebral circulation.

Adult↗
PubMed1997

Insights into the mechanism of the nitroprusside-induced increase in cardiac output in failing hearts: an attempt at its prediction with Doppler echocardiography.

Increased left ventricular (LV) diastolic pressure is consistently decreased by the administration of nitroprusside; however, nitroprusside-induced changes in cardiac output (CO) vary among patients with failing hearts. Although the variation has been considered to be related to interindividual inhomogeneity of LV diastolic performance, nitroprusside-induced changes in CO are not predictable before drug administration in individual subjects. We attempted to clarify whether nitroprusside-induced changes in CO may be predicted by analysis of the mitral flow velocity pattern in failing hearts. LV diastolic pressure was increased by the combination of the decrease in LV function and the volume expansion, and 15 conditions with LV end-diastolic pressure (EDP) > or =15 mm Hg were obtained in 8 dogs. In each condition, pulsed Doppler mitral flow velocity patterns were recorded simultaneously with hemodynamic variables before and during intravenous nitroprusside infusion. After nitroprusside administration, LV systolic pressure and LVEDP decreased in all dogs, and CO increased in eight conditions but decreased in seven conditions. CO was more likely to increase with administration of nitroprusside, and its change was greater in the conditions in which deceleration time of the early diastolic filling wave before nitroprusside infusion was longer (r = 0.56, p<0.05, n = 15). Better correlation was obtained with multiple-regression analysis, using the deceleration time and peak filling velocity at atrial contraction (r = 0.67, p<0.05, n = 15). The deceleration time correlated with LV dynamic compliance (r = 0.66, p<0.01, n = 30). Analysis of mitral flow velocity patterns may be useful in predicting nitroprusside-induced changes in CO in failing hearts.

Animals↗
PubMed1980

Sodium nitroprusside induced cGMP accumulation in isolated frog skin epithelium. Effect on cAMP, hydroosmotic and natriferic response to antidiuretic horomone.

UNLABELLED: The cGMP content of isolated frog skin epithelia has been measured, and the basal level was found to be 14.3 +/- 1.7 fmol/mg dry lweight. 0.1 mM sodium nitroprusside induced a 10-fold increase in the cGNP level within 5 min after which it rose more slowly. The maximum increase in cGMP level was obtained with 1 mM sodium nitroprusside, giving a 20-50-fold increase. 1 mM sodium nitroprusside per se had no effect on osmotic water flow or active sodium transport. On the other hand, the osmotic water flow response to arginine vasotocin was somewhat enhanced in skins which had been pretreated with 1 mM sodium nitroprusside; thus the water flow responses to 1 and 31 ng/ml arginine vasotocin were on the average 31 and 14% higher in skins exposed to sodium nitroprusside than in control skins. Sodium nitroprusside had no effect on the increment in sodium transport rate elicited by arginine vasotocin. Sodium nitroprusside alone increased the cAMP level slightly; the enhanced cAMP level, reached after 30 min incubation with 40 ng/ml arginine vasotocin, was 20% higher in the presence of 1 mM sodium nitroprusside. IN CONCLUSION: cGMP has no effect on osmotic water flow nor on active sodium transport and is not involved in the regulation of sodium transport by antidiuretic hormone. However, cGMP (or sodium nitroprusside) has a moderate effect on the hormone-stimulated osmotic water flow.

Animals↗
PubMed1977

Comparison of nitroglycerin-, nitroprusside-, and phentolamine-induced changes in coronary collateral function in dogs.

The recent use of vasodilators to improve ventricular function in acute myocardial infarction led us to investigate the effects of nitroglycerin, nitroprusside, and phentolamine on coronary collateral flow. Dogs were studied 2-4 wk after an ameroid constrictor was placed around the left anterior descending (LAD) coronary artery. Retrograde flow and peripheral coronary pressure were measured from a cannula inserted in the LAD distal to the ameroid. Systemic arterial pressure was held constant by an aortic cuff. When administered intracoronary (i.c.), nitroglycerin, 0.3-100 mug/min, or nitroprusside, 3-100 mug/min, produced quantitatively similar, dose-dependent increases in retrograde flow. Neither drug, i.c., changed peripheral coronary pressure. Nitroglycerin, 3-300 mug/min, intravenous (i.v.), produced dose-dependent increases in retrograde flow; nitroprusside, i.v., increased retrograde flow only in high doses (100-300 mug/min). Nitroglycerin and nitroprusside, i.v., produced similar increases in peripheral coronary pressure. Phentolamine, 1-300 mug/min, i.v., decreased retrograde flow, and did not change peripheral coronary pressure. Nitroprusside was considerably more potent than nitroglycerin in decreasing systemic arterial pressure and in reducing total coronary resistance. Thus, (a) although i.c. nitroglycerin and nitroprusside produce similar effects on collateral function, i.v. nitroglycerin is more effective than i.v. nitroprusside in augmenting collateral flow; (b) phentolamine has deleterious effects on collateral function; and (c) the relative vasodilator potencies of nitroglycerin and nitroprusside vary in different vascular beds; thus, for a given reduction in systemic arterial pressure, nitroprusside is less effective in increasing retrograde flow.

Animals↗
PubMed1984

The effects of sodium nitroprusside on the phasic and tonic contraction of the potassium contracture of the smooth muscle of guinea-pig vas deferens and portal vein.

The effects of sodium nitroprusside on potassium-induced phasic and tonic contraction of the guinea pig vas deferens and portal vein were studied. Sodium nitroprusside at concentrations higher than 10(-4) M potentiated the phasic contraction of potassium contracture of the vas deferens, while it showed no or slight depressing effect on the tonic contraction. Sodium nitroprusside at the same concentration depressed both the phasic and tonic contractions of the portal vein. Sodium nitroprusside depolarized the membrane of the vas deferens but did not alter the depolarization by K-Tyrode's solution. Potentiation of the phasic contraction was also observed following the pretreatment with 20 mM K+. When sodium nitroprusside was applied during the course of the tonic contraction, marked relaxation was observed in the portal vein, while only slight relaxation was induced in the vas deferens even by high concentrations of the drug. Residual tension in the presence of sodium nitroprusside was completely abolished by the application of verapamil of the concentration higher than 10(-6) M. Relaxations of preparation by sodium nitroprusside were counteracted by increases in Ca concentration. When sodium nitroprusside was applied in the presence of moderately elevated-K+ (15 to 30 mM), an increase in tension was observed in the vas deferens and a decrease in tension was observed in the portal vein. The differences in the action of sodium nitroprusside on the vas deferens and on the portal vein may be explained by the differences in the action of the drug on cell membrane, especially on the membrane potential.

Animals↗
PubMed1977

Determination of cyanide and nitroprusside in blood and plasma.

A procedure was refined for quantitative isolation of cyanide by gas transfer from acidified blood or plasma samples. The cyanide was trapped in dilute alkali and quantified as the pyridine/pyrazolone complex. The within-day coefficient of variation was 2%, which increased to about 2.5% for the day-to-day variation. Nitroprusside used as a hypotensive agent in clinical medicine provides a risk of cyanide toxicity when the rate of administration or the total amount of drug given is excessive. A procedure was developed for measuring nitroprusside in the plasma of man and animals. Nitroprusside in the sample is quantitatively converted to cyanide by incubation with cystein solution at slightly alkaline pH. Methemoglobin is added to combine with the cyanide formed and prevent its destruction. On acidification, the total amount of cyanide originally present as free cyanide or as nitroprusside is liberated as HCN, isolated by gas transfer into a sodium hydroxide trap, and quantified by spectrophotometry. Nitroprusside present in the sample is calculated from the increase in cyanide observed in the cysteine-treated sample compared to that obtained without cysteine treatment. The method has been used to estimate in vitro stability of nitroprusside in aqueous solution, blood, and plasma. Blood cyanide and plasma nitroprusside concentrations were measured when sodium nitroprusside was infused into a baboon. Over 90% of the nitroprusside in blood is present in the plasma, suggesting that the drug crosses the erythrocyte membrane slowly.

Analysis of Variance↗
PubMed1983

Comparison of the effects of nitroprusside and nitroglycerin on coronary size.

Nitroglycerin and nitroprusside are known to differ in their relative degree of systemic arterial and venous dilation. Nitroglycerin has been shown to be a potent large-vessel coronary dilator, but the effects of nitroprusside on coronary artery size are unclear. Accordingly, we studied coronary artery angiographic responses to both nitroprusside and nitroglycerin in 12 patients. Diameters Of left coronary artery segments were measured by quantitative angiography before and during an intravenous infusion of nitroprusside and after sublingual nitroglycerin when both drugs were administered in doses adjusted to achieve reductions in aortic pressure. Dilation of the left coronary artery was observed after nitroprusside and after nitroglycerin. Degrees of dilation were similar in the various left coronary artery segments after either nitroprusside or nitroglycerin. In general, segments located more proximally dilated less than those located more distally after either agent. We conclude that both nitroprusside and nitroglycerin are potent dilators of large epicardial and of smaller intramuscular coronary artery segments. The magnitude of dilation of all measured left coronary artery segments appeared remarkably similar with nitroprusside and nitroglycerin given in doses that produced a similar reduction in aortic pressure.

Angiography↗
PubMed1996

Cell death, survival and proliferation in Tetrahymena thermophila. Effects of insulin, sodium nitroprusside, 8-Bromo cyclic GMP, NG-methyl-L-arginine and methylene blue.

Cells of the ciliate Tetrahymena thermophila produce compounds that act as autocrine (paracrine) survival and/or growth factors. 8-Bromo cyclic GMP, sodium nitroprusside, hemin, protoporphyrin IX, human recombinant and bovine insulin were tested for their ability to substitute for the cell-produced factors and stimulate cell survival and proliferation. The cells were inoculated into conical flasks in a nutritionally complete, chemically defined medium at known cell densities from 5 to 5000 cells/ml. In unsupplemented medium cells at 5 to 500 cells/ml ('low initial cell density cultures') died within 8 h, whereas cells at 1000 and 5000 cells/ml ('high initial cell density cultures') proliferated with lag phases lasting for up to 4 h. In the presence of insulin compounds, hemin, protoporphyrin IX, or 8-bromo cyclic GMP, cells also proliferated at all low initial cell densities. Sodium nitroprusside was effective over two separate concentration ranges: at the nanomolar levels as well at low pico- to femtomolar levels. At initial population densities of up to 50 cells/ml the cells at both concentrations of sodium nitroprusside survived about 4-fold longer than the controls. At 500 initial cells/ml, cells at the high concentrations of sodium nitroprusside survived about 4-fold longer than those of the control cultures; they proliferated in the low concentrations of sodium nitroprusside. Concentrations of hemin, too low to have any effects on their own, had synergistic effects with sodium nitroprusside. NG-methyl-L-arginine inhibited proliferation at high initial cell densities. This inhibitory action was reduced by high concentrations of L-arginine, protoporphyrin IX, sodium nitroprusside, or 8-bromo cGMP, but not by insulin. Methylene blue inhibited cell proliferation at high initial cell densities. This inhibition was circumvented by addition of 8-bromo cGMP. The findings that insulin-related material may be released from Tetrahymena and that insulin and sodium nitroprusside increase intracellular cGMP in these cells are discussed in relation to the presented results. Together these observations suggest that cGMP is responsible for supporting cell survival in Tetrahymena and switching the cells into their proliferative mode, and that cell-produced signal molecules and insulin stimulate an NO-dependent guanylate cyclase into producing cGMP.

Animals↗
PubMed1975

Mode of action of sodium nitroprusside on vascular smooth muscle.

1. Sodium nitroprusside is a potent relaxant of smooth muscles with a predominantly tonic response, e.g. rat aorta contracted by noradrenaline, angiotensin II, Phe2-Lys8-vasopressin, BaC1(2), or KC1, and guinea-pig tracheal smooth muscle contracted by carbachol. 2. Smooth muscle preparations from the splanchnic region and with varying degrees of phasic contractility are less sensitive and develop tachyphylaxis (portal vein, duodenum of the rat) or are unresponsive to sodium nitroprusside (vas deferens, uterus of the rat). 3. Cardiac auricles of the guinea pig are not affected by sodium nitroprusside in either frequency or amplitude or spontaneous contractions. 4. Sdium nitroprusside causes a parallel shift of the dose-response curve of rat aorta to noradrenaline to the right and reduces the maximum response. 5. The drug has no blocking or stimulant effect on alpha- or beta-adrenoceptors, respectively. 6. Sodium nitroprusside inhibits the contractile response of calcium-depleted depolarized rat aorta to extra-cellular calcium. Like verapamil, it inhibits the increment in 45calcium uptake of rabbit aorta elicited by K+. Sodium nitroprusside significantly reduced 45calcium binding by microsomes prepared from rabbit aorta. 7. Rabbit aorta was incubated with lanthanum chloride to prevent calcium influx; sodium nitroprusside reduced the maintained rapid contraction phase in response to noradrenaline which is believed to be based on the intracellular activation of calcium. 8. In rat aorta, cellular cAMP and ATP levels were not found to be affected by the drug. 9. Rabbit aorta, "skinned" by glycerination is unresponsive to sdoium nitroprusside. 10. It is concluded that sodium nitropruside acts on exictation-contraction coupling predominantly in tonic smooth muscle by interfering with both the influx and the intracellular activation of calcium.

Adenosine Triphosphate↗